J M Pericàs1, J A Messina2, C Garcia-de-la-Mària1, L Park3, B K Sharma-Kuinkel4, F Marco5, D Wray6, Z A Kanafani7, M Carugati4, E Durante-Mangoni8, P Tattevin9, V H Chu2, A Moreno1, V G Fowler2, J M Miró10. 1. Infectious Diseases Service, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques Pi i Sunyer (IDIBAPS), Barcelona, Spain. 2. Division of Infectious Diseases and International Health, Duke University Medical Center, Durham, NC, USA; Duke Clinical Research Institute, Durham, NC, USA. 3. Division of Infectious Diseases and International Health, Duke University Medical Center, Durham, NC, USA; Duke Global Health Institute, Durham, NC, USA. 4. Division of Infectious Diseases and International Health, Duke University Medical Center, Durham, NC, USA. 5. Department of Microbiology, Institute for Global Health, Hospital Clinic of Barcelona, University of Barcelona, Barcelona, Spain. 6. Infectious Disease Division, Medical University of South Carolina, Charleston, SC, USA. 7. Division of Infectious Diseases, American University of Beirut, Beirut, Lebanon. 8. Internal Medicine, Department of Clinical and Experimental Medicine, University of Campania 'Luigi Vanvitelli', Italy; Unit of Infectious and Transplant Medicine, 'V. Monaldi' Hospital, AORN dei Colli, Naples, Italy. 9. Infectious Diseases and Intensive Care Unit, Pontchaillou University Hospital, Rennes, France. 10. Infectious Diseases Service, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques Pi i Sunyer (IDIBAPS), Barcelona, Spain. Electronic address: jmmiro@ub.edu.
Abstract
OBJECTIVES: Left-sided methicillin-susceptible Staphylococcus aureus (MSSA) endocarditis treated with cloxacillin has a poorer prognosis when the vancomycin minimum inhibitory concentration (MIC) is ≥1.5 mg/L. We aimed to validate this using the International Collaboration on Endocarditis cohort and to analyse whether specific genetic characteristics were associated with a high vancomycin MIC (≥1.5 mg/L) phenotype. METHODS: All patients with left-sided MSSA infective endocarditis treated with antistaphylococcal β-lactam antibiotics between 2000 and 2006 with available isolates were included. Vancomycin MIC was determined by Etest as either high (≥1.5 mg/L) or low (<1.5 mg/L). Isolates underwent spa typing to infer clonal complexes and multiplex PCR for identifying virulence genes. Univariate analysis was performed to evaluate the association between in-hospital and 1-year mortality, and vancomycin MIC phenotype. RESULTS: Sixty-two cases met the inclusion criteria. Vancomycin MIC was low in 28 cases (45%) and high in 34 cases (55%). No significant differences in patient demographic data or characteristics of infection were observed between patients with infective endocarditis due to high and low vancomycin MIC isolates. Isolates with high and low vancomycin MIC had similar distributions of virulence genes and clonal lineages. In-hospital and 1-year mortality did not differ significantly between the two groups (32% (9/28) vs. 27% (9/34), p 0.780; and 43% (12/28) vs. 29% (10/34), p 0.298, for low and high vancomycin MIC respectively). CONCLUSIONS: In this international cohort of patients with left-sided MSSA endocarditis treated with antistaphylococcal β-lactams, vancomycin MIC phenotype was not associated with patient demographics, clinical outcome or virulence gene repertoire.
OBJECTIVES: Left-sided methicillin-susceptible Staphylococcus aureus (MSSA) endocarditis treated with cloxacillin has a poorer prognosis when the vancomycin minimum inhibitory concentration (MIC) is ≥1.5 mg/L. We aimed to validate this using the International Collaboration on Endocarditis cohort and to analyse whether specific genetic characteristics were associated with a high vancomycin MIC (≥1.5 mg/L) phenotype. METHODS: All patients with left-sided MSSA infective endocarditis treated with antistaphylococcal β-lactam antibiotics between 2000 and 2006 with available isolates were included. Vancomycin MIC was determined by Etest as either high (≥1.5 mg/L) or low (<1.5 mg/L). Isolates underwent spa typing to infer clonal complexes and multiplex PCR for identifying virulence genes. Univariate analysis was performed to evaluate the association between in-hospital and 1-year mortality, and vancomycin MIC phenotype. RESULTS: Sixty-two cases met the inclusion criteria. Vancomycin MIC was low in 28 cases (45%) and high in 34 cases (55%). No significant differences in patient demographic data or characteristics of infection were observed between patients with infective endocarditis due to high and low vancomycin MIC isolates. Isolates with high and low vancomycin MIC had similar distributions of virulence genes and clonal lineages. In-hospital and 1-year mortality did not differ significantly between the two groups (32% (9/28) vs. 27% (9/34), p 0.780; and 43% (12/28) vs. 29% (10/34), p 0.298, for low and high vancomycin MIC respectively). CONCLUSIONS: In this international cohort of patients with left-sided MSSA endocarditis treated with antistaphylococcal β-lactams, vancomycin MIC phenotype was not associated with patient demographics, clinical outcome or virulence gene repertoire.
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